Interestingly, EGFR inhibition with afatinib led to increased levels of p-STAT3 Y705 in both BT50 (EGFR wt) and BT73 (EGFRvIII mt) (Figure 1D and Supplementary Figure S1E), but not in p-AKT or p-MAPK (through a TNF activation response), which have also been previously described as possible mechanisms of resistance following EGFR inhibition in lung cancer30 and glioma,31 respectively (Figure 1D). The gene discussed is AKT1; the disease is central nervous system cancer.